Regulation of CD4+CD8−CD25+ and CD4+CD8+CD25+ T cells by gut microbiota in chicken

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作者
In Kyu Lee
Min Jeong Gu
Kwang Hyun Ko
Suhan Bae
Girak Kim
Gwi-Deuk Jin
Eun Bae Kim
Young-Yun Kong
Tae Sub Park
Byung-Chul Park
Hyun Jung Jung
Seung Hyun Han
Cheol-Heui Yun
机构
[1] Seoul National University,Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences
[2] College of Animal Life Science,Department of Animal Life Science
[3] Kangwon National University,School of Biological Sciences
[4] Seoul National University,Graduate School of International Agricultural Technology and Institute of Green Bio Science Technology
[5] Seoul National University,Department of Oral Microbiology and Immunology
[6] National Institute of Animal Science,Center for Food Bioconvergence
[7] School of Dentistry,undefined
[8] Seoul National University,undefined
[9] Seoul National University,undefined
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摘要
The gut microbiota in chicken has long been studied, mostly from the perspective of growth performance. However, there are some immunological studies regarding gut homeostasis in chicken. Although CD4+CD25+ T cells are reported to act as regulatory T cells (Tregs) in chicken, there have been no studies showing the relationship between gut microbiota and Tregs. Therefore, we established a model for ‘antibiotics (ABX)-treated chickens’ through administration of an antibiotic cocktail consisting of ampicillin, gentamycin, neomycin, metronidazole, and vancomycin in water for 7 days. CD4+CD8−CD25+ and CD4+CD8+CD25+ T cells in cecal tonsils were significantly decreased in this model. Gram-positive bacteria, especially Clostridia, was responsible for the changes in CD4+CD8−CD25+ or CD4+CD8+CD25+ T cells in cecal tonsils. Feeding ABX-treated chickens with acetate recovered CD4+CD8−CD25+ and CD4+CD8+CD25+ T cells in cecal tonsils. GPR43, a receptor for acetate, was highly expressed in CD4+CD8−CD25+ T cells. In conclusion, our study demonstrated that the gut microbiota can regulate the population of CD4+CD8−CD25+ and CD4+CD8+CD25+ T cells, and that acetate is responsible for the induction of CD4+CD8−CD25+ T cells in cecal tonsils via GPR43.
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